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Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

ABSTRACT: The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed.

ORGANISM(S): Mus musculus

PROVIDER: GSE66069 | GEO | 2015/07/10

SECONDARY ACCESSION(S): PRJNA276077

REPOSITORIES: GEO

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Analysis of Blimp-1 and Irf-1 genomic binding in wild type and Prdm1/Blimp-1 mutant embryonic gut

Project description:The goal of this study was to profile Blimp1 binding in E18.5 small intestine using a Blimp-1-eGFP knock-in allele, and to compare Blimp-1-eGFP genomic binding with Irf-1 genomic binding in normal small intestine. Changes in Irf-1 binding between wild type and Prdm1/Blimp-1 mutant small intestine were also assessed. ChIP-seq was performed for Blimp-1-eGFP in duplicate in E18.5 small intestine expressing the fusion protein using anti-GFP antibody. As a negative control a single anti-GFP ChIP was also performed in wild type small intestine. ChIP-seq for Irf-1 was performed in duplicate in both wild type and Prdm1/Blimp-1 mutant E18.5 small intestine using an anti-Irf-1 antibody. Duplicate IgG ChIP control in wild types was performed as a negative control. All samples had an associated input chromatin sample sequenced.

2015-07-10 | E-GEOD-66069 | biostudies-arrayexpress

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [ChIP-seq]

Project description:To identify candidate Blimp1 target genes in maternal decidua we performed GFP antibody ChIP-seq analysis of E6.5 decidua from homozygous female EGFP-BLIMP1 mice that express an endogenous N-terminal EGFP-tagged Blimp1 protein (Mitani et al., 2017).

2020-05-01 | GSE141611 | GEO

Blimp-1 moulds the epigenetic architecture of IL-21-mediated autoimmune diseases through an autoregulatory circuit

Project description:To unravel how Blimp-1 systematically manipulates the global transcriptional landscape in CD4 T cells to contribute to autoimmune progression, we performed RNA sequencing analysis in Blimp-1 transgenic (BTg) or Blimp1-deficient (CKO) NOD mice

2022-12-31 | GSE200545 | GEO

The transcriptional repressor Blimp-1/Prdm1 controls the maternal decidual response during pregnancy [RNA-seq]

Project description:Transcriptional profiling of E5.5 and E6.5 wild type and Blimp1 mutant decidua was performed using RNA-seq to identify maternal Blimp1 functions during pregnancy .

2020-05-01 | GSE141612 | GEO

The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes

Project description:Expression profiling of Prdm1 mutant E18.5 small intestine was performed using Illumina whole genome V2 arrays. The hypothesis tested in the present study was that Blimp1 regulates the transcription of key genes involved in enterocyte differentiation and survival. Results identify substantial and premature activation of key components of the adult enterocyte biochemical signature. Villin-Cre and Prdm1BEH/+ animals were intercrossed to generate heterozygous Villin-Cre, Prdm1BEH males that were then mated with homozygous Prdm1 CA/CA females carrying the R26R allele to generate Prdm1+/+ (Prdm1CA/+) or Prdm1-/- (Villin-Cre, Prdm1CA/BEH) offspring. Total RNA obtained from 11 Prdm1+/+ and 10 Prdm1-/- E18.5 small intestine samples was hybridized to Illumina WG6_V2 beadchips.

2011-06-02 | E-GEOD-29658 | biostudies-arrayexpress

The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes

2011-06-02 | GSE29658 | GEO

Epigenetic modifications induced by Blimp-1 regulate CD8+ T cell memory progression during acute virus infection

Project description:Blimp-1 regulates the overall accumulation of virus-specific CD8+ T cells during acute viral infections. Increased proliferation and survival of Blimp-1-deficient CD8+ T cells is promoted by persistent cytokine responsiveness, resulting from sustained expression of CD25 and CD27. Knockdown of these genes reduced the Blimp-1-deficient CD8+ T cell response. Genome-wide ChIP-sequencing analysis identified CD25 and CD27 genes as direct targets of Blimp-1. At the peak of the anti-viral response, but not earlier, Blimp-1 recruited the histone modifying enzymes G9a and HDAC2 to the Il2ra and Cd27 loci, thereby repressing expression of these genes. In the absence of Blimp-1, the Il2ra and Cd27 genes exhibited enhanced histone H3-acetylation and reduced histone H3K9-trimethylation. These data elucidate a central mechanism by which Blimp-1 acts as an epigenetic regulator, enhancing the numbers of short-lived effector cells while suppressing the development of memory precursor CD8+ T cells. NaM-CM-/ve CD8+ T cells from OT-I TCR transgenic Rag1-/- mice were stimulated with anti-CD3 and anti-CD28 for three days in vitro, in the presence of IL-2 to up-regulate Blimp-1 protein. Genome-wide mapping of Blimp-1 binding in mouse CD8+ T cells was conducted.

2013-10-10 | E-GEOD-48358 | biostudies-arrayexpress

miRNA expression in Blimp-1-deficient dendritic cells

Project description:Expression of Blimp-1 was specifically deleted in dendritic cells (DCs) by breeding Blimp-1 flox and CD11c-CRE mice. MiRNA expression was evaluated and compared from DCs, CD4+ T cells and total B cells from spleens of control and Blimp-1 KO mice. Age-matched (6-10 weeks old) female mice from control and Blimp-1 KO mice were sacrificed and spleens were collected. CD11chi/MHCIIhi DCs, CD4+TCRb+ T cells and B220+ B cells were sorted by FACSaria. MiRNA was measured from the total RNA preparation.

2013-09-05 | E-GEOD-40587 | biostudies-arrayexpress

Cooperation of IRF-4 and IRF-8 deficiencies in the development of hematological malignancies

Project description:We found that mice deficient in both IRF-4 and IRF-8 develop from a very early age a more aggressive CML-like disease than mice deficient in IRF-8 alone. IRF-4 deficiency dramatically enhanced the effect of IRF-8 deficiency on expansion of granulocyte-monocyte progenitors (GMPs). All mice deficient in both IRF-4 and IRF-8 eventually develop and succumb to a B-lymphoblastic leukemia/lymphoma at approximately 25 weeks of age. The results demonstrate that IRF-4 and IRF-8 deficiencies can cooperate in the development of both myeloid and lymphoid tumors. To gain insights into how loss of IRF-4 affects the transcriptional program underlying leukemogenesis, we analyzed the genome-wide transcription profiles of GMPs from WT, IRF-8 KO and IRF-4/8 DKO mice. Microarray analysis revealed genes differentially expressed in IRF-4/8 DKO and IRF-8 KO GMPs, including genes that are involved in cell growth regulation and/or tumorigenesis.

2010-08-22 | GSE21018 | GEO

The roles of IRF-3 and IRF-7 in innate antiviral immunity against dengue virus

Project description:We investigated the roles of IRF-3 and IRF-7 in innate antiviral immunity against dengue virus (DENV). Double-deficient Irf-3-/-7-/- mice infected with the DENV2 strain S221 possessed 1,000-150,000 fold higher levels of viral RNA than wild-type and single-deficient mice 24 hours after infection; however, they remained resistant to lethal infection. IFN-α/β was induced similarly in wild-type and Irf-3-/- mice post DENV infection, whereas in the Irf-7-/- and Irf-3-/-7-/- mice, significantly low levels of IFN-α/β expression was observed within 24 hours post-infection. IFN-stimulated gene (ISG) induction was also delayed in Irf-3-/-7-/- mice relative to wild-type and single-deficient mice. In particular, Cxcl10 and Ifnα2 were rapidly induced independently of both IRF-3 and IRF-7 in the Irf-3-/-7-/- mice with DENV infection. Higher levels of serum IFN-γ, IL-6, CXCL10, IL-8, IL-12 p70, and TNF were also observed in Irf-3-/-7-/- mice 24 hours after infection, at which time point viral titers peaked and started to be cleared. Antibody-mediated blockade experiments revealed that IFN-γ, CXCL10, and CXCR3 function to restrict DENV replication in Irf-3-/-7-/- mice. Additionally, the ISGs Cxcl10, Ifit1, Ifit3, and Mx2 can be induced via an IRF-3- and IRF-7-independent pathway that does not involve IFN-γ signaling for protection against DENV. Collectively, these results demonstrate that IRF-3 and IRF-7 are redundant, albeit IRF-7 plays a more important role than IRF-3 in inducing the initial IFN-α/β response; only the combined actions of IRF-3 and IRF-7 are necessary for efficient control of early DENV infection; and the late, IRF-3- and IRF-7-independent pathway contributes to anti-DENV immunity.

2013-08-15 | GSE49871 | GEO

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